Infectious agents, particularly viruses, have long been thought to play a role in the pathogenesis of the sudden infant death syndrome (SIDS) because of epidemiological, serological and virus culture studies. However, no morphologically demonstrable lesion of sufficient magnitude to cause death has been shown in SIDS in association with viral (or other) infections. In fact, such a demonstration excludes the diagnosis of SIDS. Thus, if an infectious process is significant in the mechanism of SIDS deaths, it seems that it must act in a previously unrecognized manner. Our objective is to determine if intravascular cellular aggregation, whether from hemagglutination, hemadsorption, platelet aggregation, or disseminated intravascular coagulation (DIC) secondary to endotoxemia, is present in cases of SIDS. Our goals for the coming year include continuing to measure pO2, immune parameters, viral studies, and electron microscopic examination of the pulmonary vasculature in cases of SIDS. We will also measure osmotic fragility and study the proteins from red cell membranes with polyacrylamide gel electrophoresis to define membrane changes which could accompany red cell abnormalities. BIBLIOGRAPHIC REFERENCES: Mason, James M., Mason, Linda H., Jackson, Michael, Bell, James S., Francisco, J.T., and Jennings, B.R. 1975. Pulmonary Vessels in SIDS. New England Journal of Medicine, 292 (9): 479.